Objective: The objective of the study was to evaluate the effect of ethyl pyruvate (EP) in ameliorating liver injury in rats with severe acute pancreatitis (SAP) and its possible mechanism.
Methods: Rats were randomly divided into control group, SAP group, and EP-treated group. Then, the tissue specimens were harvested for morphological studies, immunohistochemistry examination, reverse transcriptase-polymerase chain reaction, and Western blot analysis. The DNA-binding activity of nuclear factor κB was measured by electrophoretic mobility shift assay. The concentrations of serum amylase, alanine aminotransferase, and pancreatic tissue malondialdehyde and the activity of myeloperoxidase in the liver were determined.
Results: Treatment with EP after SAP was associated with a reduction in the severity of SAP and liver injury. Treatment with EP significantly decreased the hepatic mRNA expression of tumor necrosis factor α and interleukin 1β and ameliorated the activity of myeloperoxidase in the liver in SAP rats. Compared with the SAP group, treatment with EP significantly decreased the infiltration of inflammatory cells and markedly inhibited hepatic nuclear factor κB DNA binding; EP therapy dramatically inhibited high-mobility group box 1 expression from inflamed hepatic tissue.
Conclusions: Our results demonstrate that EP might play a therapeutic role in liver inflammation in this SAP model, and these beneficial effects of EP are because of the modulation of high-mobility group box 1 and other inflammatory cytokine responses.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1097/MPA.0b013e31823cd3ef | DOI Listing |
Alcohol Clin Exp Res (Hoboken)
January 2025
Department of Anatomy, Yonsei University Wonju College of Medicine, Wonju, Korea.
Background: Therapeutic options for managing intestinal and hepatic inflammation associated with alcohol consumption, a prevalent health problem worldwide, remain unavailable. This study examines the potential efficacy of polyethylene glycol (PEG) in mitigating the intestinal and hepatic damage, employing a mouse model for assessment.
Methods: First, the mixture of ethanol (4 g/kg body weight) and PEG (2 g/kg body weight) or an equivalent volume of vehicle was administered orally alcohol consumption.
J Clin Gastroenterol
December 2024
Department of Infectious Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Aim: To compare the respective clinical and pathologic features of antimitochondrial antibodies-negative (AMA-negative) primary biliary cirrhosis (PBC) and cholestatic type drug-induced liver injury (DILI) for clinical differential diagnosis.
Patients And Methods: Clinical data from 23 patients with AMA-negative PBC and 39 patients with cholestatic type DILI, treated at our hospital between January 2013 and January 2024, were collected and retrospectively analyzed.
Results: The cholestatic type DILI group exhibited a higher incidence of malaise and abdominal pain compared with the AMA-negative PBC group.
Hepatol Commun
November 2024
Human Immunology Laboratory, School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Camperdown, New South Wales, Australia.
Background: HCC develops in the context of chronic inflammation; however, the opposing roles the immune system plays in both the development and control of tumors are not fully understood. Mapping immune cell interactions across the distinct tissue regions could provide greater insight into the role individual immune populations have within tumors.
Methods: A 39-parameter imaging mass cytometry panel was optimized with markers targeting immune cells, stromal cells, endothelial cells, hepatocytes, and tumor cells.
Hepatol Commun
November 2024
Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Background: Overdose of acetaminophen (APAP), a commonly used antipyretic analgesic, can lead to severe liver injury and failure. Current treatments are only effective in the early stages of APAP-induced acute liver injury (ALI). Therefore, a detailed examination of the mechanisms involved in liver repair following APAP-induced ALI could provide valuable insights for clinical interventions.
View Article and Find Full Text PDFHepatol Commun
November 2024
Department of Medicine, University of California, San Diego, La Jolla, California, USA.
Background: Liver fibrosis is caused by chronic toxic or cholestatic liver injury. Fibrosis results from the recruitment of myeloid cells into the injured liver, the release of inflammatory and fibrogenic cytokines, and the activation of myofibroblasts, which secrete extracellular matrix, mostly collagen type I. Hepatic myofibroblasts originate from liver-resident mesenchymal cells, including HSCs and bone marrow-derived CD45+ collagen type I+ expressing fibrocytes.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!